The intestinal tumor multiplicity in mice heterozygous for APc(Min) is
strongly modulated by genetic background. On the sensitive C57BL/6J (
B6) background, mice develop large numbers of intestinal adenomas. The
AKR/J (AKR) strain carries alleles that correlate with a strong reduc
tion in tumor multiplicity. To study the effect of one of these modifi
ers, it Mom1, we have generated a mouse line in which the AKR allele o
f Mom1 is carried on the sensitive B6 genetic background. This strain
was produced by using a marker-assisted selection method to eliminate
unlinked AKR alleles more rapidly. The application and efficiency of t
his method are discussed. We used this strain to determine that Mom1 a
ffects both tumor multiplicity and tumor size in a semi-dominant fashi
on.